Editorial
Circular non-coding RNAs in diabetic retinopathy
Abstract
Diabetes mellitus is a pandemic disease currently affecting more than 400 million people worldwide (1). The common symptom of Diabetes is hyperglycemia. Chronically elevated blood glucose concentrations result in severe morbidities such as cardiac infarction, stroke, nephropathy, neuropathy and retinopathy primarily caused by micro- and macrovascular dysfunctions (1). Diabetic retinopathy (DR) is a multi-stage disease with a complex pathogenesis comprising changes in function and/or viability of several cell types such as pericytes, vascular endothelial cells, glial cells, neuronal cells and immune cells (2,3). Clinically the first symptoms of a beginning DR are presented as microaneurysms of the retinal vasculature and neuronal dysfunctions with not yet detectable neurodegeneration (2,3). The underlying cause of this disease is still subject of research and involves, amongst other reasons, formation of reactive oxygen species (ROS), reactive metabolites, activation of protein kinase C and the hexosamine pathway (3,4). However, given the complexity of retinal retinopathy, which currently affects ~one-third of people with type 2 diabetes and its temporal disease stages other players, such as non-coding RNAs (ncRNAs) might also play a role.